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Metabolic Disturbances (metabolic + disturbance)
Selected AbstractsLinking obesity to colorectal cancer: Application of nutrigenomicsBIOTECHNOLOGY JOURNAL, Issue 9 2010Professor Mi-Kyung Sung Abstract Diet is one of the most affective environmental factors in cancer development. Due to complicated nature of the diet, it has been very difficult to provide clear explanations for the role of dietary components in carcinogenesis. However, as high-throughput omics techniques became available, researchers are now able to analyze large sets of gene transcripts, proteins, and metabolites to identify molecules involved in disease development. Bioinformatics uses these data to perform network analyses and suggest possible interactions between metabolic processes and environmental factors. Obesity is known as one of the most closely related risk factors of colorectal cancer (CRC). Metabolic disturbances due to a positive energy balance may trigger and accelerate CRC development. In this review, we have summarized reports on genes, proteins and metabolites that are related to either obesity or CRC, and suggested candidate molecules linking obesity and CRC based on currently available literature. Possible application of bioinformatics for a large scale network analysis in studying cause-effect relationship between dietary components and CRC are suggested. [source] Hypercalcemia and Overexpression of CYP27B1 in a Patient With Nephrogenic Systemic Fibrosis: Clinical Vignette and Literature Review,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 6 2009Vivian Y Pao Abstract Nephrogenic systemic fibrosis (NSF) is a disease of thickened, hard, hyperpigmented skin lesions with or without systemic fibrosis occurring in patients with renal insufficiency and associated with the administration of gadolinium-containing contrast. The pathogenesis of this disease is unclear, and there is no definitive treatment. We describe a 71-yr-old patient with stable chronic lymphocytic leukemia (CLL), end-stage renal disease (ESRD), and NSF who presented with hypercalcemia in 2006. Before onset of renal insufficiency in 2002, serum calcium, phosphorus, and PTH levels were normal. In 2004, the patient began hemodialysis, and he was diagnosed with NSF in 2005, shortly after undergoing an MRI with gadolinium contrast administration. Over the next 6 mo, albumin-corrected serum total calcium levels rose from 9.9 to 13.1 mg/dl (normal range, 8.5,10.5 mg/dl) with normal serum phosphorus levels. On admission in September 2006, 1,25-dihydroxyvitamin D [1,25(OH)2D] levels were elevated at 130.7 pg/ml (normal range, 25.1,66.1 pg/ml). Biopsy of an NSF lesion showed increased 25-hydroxyvitamin D3,1-, hydroxylase (CYP27B1) immunostaining compared with the biopsy from a normal control. This is the first reported association of NSF with hypercalcemia caused by elevated 1,25(OH)2D levels. This metabolic disturbance should be sought in future cases to determine a connection between NSF, 1,25(OH)2D metabolism, and CYP27B1 activation in the skin, which may shed light on the pathogenesis of this unusual local and systemic fibrosing disorder. [source] Sodium valproate inhibits glucose transport and exacerbates Glut1-deficiency in vitroJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2005Hei Yi Wong Abstract Anticonvulsant sodium valproate interferes with brain glucose metabolism. The mechanism underlying such metabolic disturbance is unclear. We tested the hypothesis that sodium valproate interferes with cellular glucose transport with a focus on Glut1 since glucose transport across the blood-brain barrier relies on this transporter. Cell types enriched with Glut1 expression including human erythrocytes, human skin fibroblasts, and rat astrocytes were used to study the effects of sodium valproate on glucose transport. Sodium valproate significantly inhibited Glut1 activity in normal and Glut1-deficient erythrocytes by 20%,30%, causing a corresponding reduction of Vmax of glucose transport. Similarly, in primary astrocytes as well as in normal and Glut1-deficient fibroblasts, sodium valproate inhibited glucose transport by 20%,40% (P,<,0.05), accompanied by an up to 60% downregulation of GLUT1 mRNA expression (P,<,0.05). In conclusion, sodium valproate inhibits glucose transport and exacerbates Glut1 deficiency in vitro. Our findings imply the importance of prudent use of sodium valproate for patients with compromised Glut1 function. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source] Visceral fat mass as a marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndromeBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2 2007JP Marasinghe No abstract is available for this article. [source] Authors response to: Visceral fat mass as a marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndromeBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2 2007J Lord No abstract is available for this article. [source] An 11-year experience of enterocutaneous fistula,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 12 2004P. Hollington Background: Enterocutaneous fistula has traditionally been associated with substantial morbidity and mortality, related to fluid, electrolyte and metabolic disturbance, sepsis and malnutrition. Methods: A retrospective review of enterocutaneous fistula in 277 consecutive patients treated over an 11-year period in a major tertiary referral centre was undertaken to evaluate current management practice and outcome. Results: Most fistulas occurred secondary to abdominal surgery, and a high proportion (52·7 per cent) occurred in association with inflammatory bowel disease. A low rate of spontaneous healing was observed (19·9 per cent). The healing rate after definitive fistula surgery was 82·0 per cent, although more than one attempt was required to achieve surgical closure in some patients. Definitive fistula resection resulted in a mortality rate of 3·0 per cent. In addition, one patient died after laparotomy for intra-abdominal sepsis and an additional 24 patients died from complications of fistulation, giving an overall fistula-related mortality rate of 10·8 per cent. Conclusion: Early recognition and control of sepsis, management of fluid and electrolyte imbalances, meticulous wound care and nutritional support appear to reduce the mortality rate, and allow spontaneous fistula closure in some patients. Definitive surgical management is performed only after restitution of normal physiology, usually after at least 6 months. Copyright © 2004 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Selective glucocorticoid receptor (type II) antagonist prevents and reverses olanzapine-induced weight gainDIABETES OBESITY & METABOLISM, Issue 6 2010J. K. Belanoff Use of antipsychotic medications has been associated consistently with weight gain and metabolic disturbances, and a subsequent increased risk for diabetes and cardiovascular disease. Two experiments tested whether CORT 108297, a newly identified selective glucocorticoid antagonist could (i) reduce and (ii) prevent olanzapine-induced weight gain in rats. In the first experiment, rats dosed only with olanzapine gained a statistically significant amount of weight. When vehicle was added to their olanzapine dose, they continued to gain weight; when CORT 108297 was added to their regimen, they lost a significant amount of weight. Rats administered CORT 108297 plus olanzapine had significantly less abdominal fat than those who received olanzapine alone. In the second experiment, rats receiving olanzapine plus CORT 108297 gained significantly less weight than rats receiving only olanzapine. Increasing doses of CORT 108297 were associated with less weight gain. [source] Common infections in diabetes: pathogenesis, management and relationship to glycaemic controlDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2007Anton Y. Peleg Abstract Specific defects in innate and adaptive immune function have been identified in diabetic patients in a range of in vitro studies. However, the relevance of these findings to the integrated response to infection in vivo remains unclear, especially in patients with good glycaemic control. Vaccine efficacy seems adequate in most diabetic patients, but those with type 1 diabetes and high glycosylated haemoglobin levels are most likely to exhibit hypo-responsiveness. While particular infections are closely associated with diabetes, this is usually in the context of extreme metabolic disturbances such as ketoacidosis. The link between glycaemic control and the risk of common community-acquired infections is less well established but could be clarified if infection data from large community-based observational or intervention studies were available. The relationship between hospital-acquired infections and diabetes is well recognized, particularly among post-operative cardiac and critically ill surgical patients in whom intensive insulin therapy improves clinical outcome independent of glycaemia. Nevertheless, further research is needed to improve our understanding of the role of diabetes and glycaemic control in the pathogenesis and management of community- and hospital-acquired infections. Copyright © 2006 John Wiley & Sons, Ltd. [source] Evaluation of a bedside blood ketone sensor: the effects of acidosis, hyperglycaemia and acetoacetate on sensor performanceDIABETIC MEDICINE, Issue 7 2004A. S. A. Khan Abstract Aims To assess the performance of a handheld bedside ketone sensor in the face of likely metabolic disturbances in diabetic ketoacidosis, namely: pH, glucose and acetoacetate. Methods The effects of pH (7.44,6.83), glucose (5,50 mmol/l) and acetoacetate (0,5 mmol/l) were examined in venous blood to investigate the accuracy of betahydroxybutyrate measurement (0,5 mmol/l) by a handheld ketone sensor. Sensor results were compared with a reference method. Linear regression models were fitted to the difference between the methods with the concentration of metabolite as the explanatory factor. Results Decreasing pH and increasing glucose had no effect on the accuracy of the handheld ketone sensor; the gradients of the fitted lines were ,0.14 and ,0.003, respectively. The 95% confidence intervals were ,0.7,0.4 and ,0.01,0.004, respectively (P = 0.59 and 0.4, respectively). In the acetoacetate study, a positive relationship between the sensor and reference method results was found, the gradient was 0.09. The 95% confidence interval was 0.05,0.14 (P , 0.001), indicating that high concentrations of acetoacetate interfere with the sensor performance. Conclusions Acidosis and hyperglycaemia have minimal effects on the sensor performance. However, high concentrations of acetoacetate result in some overestimation of betahydroxybutyrate. This bedside ketone sensor provides useful data over a broad range of conditions likely to be encountered during moderate to severe diabetic ketoacidosis. [source] Our children and the metabolic syndromeDRUG DEVELOPMENT RESEARCH, Issue 7 2006Jean-Claude Desmangles Abstract The metabolic syndrome is a cluster of metabolic disturbances that result in an increased risk of type 2 diabetes and cardiovascular disease in adults. Despite the lack of a uniform definition of the syndrome for children, several studies have reported an overall prevalence of 3 to 4% among children. Among obese adolescents, the prevalence can be as high as 30 to 50%. Besides insulin resistance and obesity, the intrauterine environment and genetic factors also seem to play a role in the pathogenesis of the syndrome in children. In view of the current obesity epidemic and since an increasing amount of evidence shows that obesity during adolescence is significantly associated with insulin resistance, abnormal serum lipid levels, and elevated blood pressure during adulthood, there is a great need for a clear definition, for the development of screening guidelines, and for appropriate prevention and treatment strategies for the metabolic syndrome in the pediatric population. Drug Dev. Res. 67:602,606, 2006. © 2006 Wiley-Liss, Inc. [source] Adipokines in liver diseases,HEPATOLOGY, Issue 3 2009Fabio Marra Adipokines are polypeptides secreted in the adipose tissue in a regulated manner. While some of these molecules are expressed only by adipocytes, resident and infiltrating macrophages and components of the vascular stroma markedly contribute to expression of other adipokines. As a result, adipose tissue inflammation is associated with a modification in the pattern of adipokine secretion. Leptin, adiponectin, and resistin are the best-studied molecules in this class, but cytokines such as tumor necrosis factor or interleukin-6 are also secreted at high levels by the adipose tissue. Several other molecules have been recently identified and are actively investigated. Adipokines interfere with hepatic injury associated with fatty infiltration, differentially modulating steatosis, inflammation, and fibrosis. Several studies have investigated plasma levels of adiponectin in patients with nonalcoholic fatty liver disease, to establish correlations with the underlying state of insulin resistance and with the type and severity of hepatic damage. Hepatitis C is another disease where adipokines may represent a link between viral infection, steatosis, and metabolic disturbances. Identification of the mediators secreted by expanded adipose tissue and their pathogenic role is pivotal in consideration of the alarming increase in the prevalence of obesity and of the detrimental role that this condition exerts on the course of liver diseases. (HEPATOLOGY 2009.) [source] Nonconcordance between subclinical atherosclerosis and the calculated Framingham risk score in HIV-infected patients: relationships with serum markers of oxidation and inflammationHIV MEDICINE, Issue 4 2010S Parra Objectives HIV-infected patients show an increased cardiovascular disease (CVD) risk resulting, essentially, from metabolic disturbances related to chronic infection and antiretroviral treatments. The aims of this study were: (1) to evaluate the agreement between the CVD risk estimated using the Framingham risk score (FRS) and the observed presence of subclinical atherosclerosis in HIV-infected patients; (2) to investigate the relationships between CVD and plasma biomarkers of oxidation and inflammation. Methods Atherosclerosis was evaluated in 187 HIV-infected patients by measuring the carotid intima-media thickness (CIMT). CVD risk was estimated using the FRS. We also measured the circulating levels of interleukin-6, monocyte chemoattractant protein-1 (MCP-1) and oxidized low-density lipoprotein (LDL), and paraoxonase-1 activity and concentration. Results There was a weak, albeit statistically significant, agreement between FRS and CIMT (,=0.229, P<0.001). A high proportion of patients with an estimated low risk had subclinical atherosclerosis (n=66; 56.4%). In a multivariate analysis, the presence of subclinical atherosclerosis in this subgroup of patients was associated with age [odds ratio (OR) 1.285; 95% confidence interval (CI) 1.084,1.524; P=0.004], body mass index (OR 0.799; 95% CI 0.642,0.994; P=0.044), MCP-1 (OR 1.027; 95% CI 1.004,1.050; P=0.020) and oxidized LDL (OR 1.026; 95% CI 1.001,1.051; P=0.041). Conclusion FRS underestimated the presence of subclinical atherosclerosis in HIV-infected patients. The increased CVD risk was related, in part, to the chronic oxidative stress and inflammatory status associated with this patient population. [source] Is major depressive disorder a metabolic encephalopathy?HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 5 2008Brian H Harvey Abstract Metabolic encephalopathy is an acute disturbance in cellular metabolism in the brain evoked by conditions of hypoxia, hypoglycaemia, oxidative stress and/or inflammation. It usually develops acutely or subacutely and is reversible if the systemic disorder is treated. If left untreated, however, metabolic encephalopathy may result in secondary structural damage to the brain. Most encephalopathies are present with neuropsychiatric symptoms, one in particular being depression. However, mood disorders are often co-morbid with cardiovascular, liver, kidney and endocrine disorders, while increasing evidence concurs that depression involves inflammatory and neurodegenerative processes. This would suggest that metabolic disturbances resembling encephalopathy may underscore the basic neuropathology of depression at a far deeper level than currently realized. Viewing depression as a form of encephalopathy, and exploiting knowledge gleaned from our understanding of the neurochemistry and treatment of metabolic encephalopathy, may assist in our understanding of the neurobiology of depression, but also in realizing new ideas in the pharmacotherapy of mood disorders. Copyright © 2008 John Wiley & Sons, Ltd. [source] Metabolic differences between Asian and Caucasian patients on clozapine treatmentHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 4 2007Mythily Subramaniam Abstract Objective To establish if there are ethnic differences in the various metabolic disturbances that are common with clozapine treatment. Method Forty subjects (20 Asians and 20 Caucasians) with a diagnosis of schizophrenia were recruited for the study. Clozapine blood levels as well as fasting blood glucose, lipid levels, and liver function tests were established. Other clinical parameters such as blood pressure and Body Mass Index (BMI) were recorded for each patient. Results The mean clozapine dose was significantly higher in the Caucasian subjects (432.5,±,194.7,mg) as compared to the Asian subjects (175.6,±,106.9,mg) (p,<,0.001) while the mean weight-corrected dose for Asian patients was lower (3.0,±,1.9 and 5.0,±,2.1,mg/kg, respectively, p,=,0.005). There were, however, no ethnic differences in the mean plasma clozapine concentration (415.3,±,185.8,ng/ml in Caucasians and 417.1,±,290.8,ng/ml in Asians). BMI were significantly higher in Caucasians, as were the number of subjects with hypertension; levels of hepatic enzymes were higher in the Asian group. Conclusions Not only are there pharmacokinetic differences between Asian and Caucasian patients receiving clozapine, but there may also be differential emergence of certain metabolic abnormalities like hypertension and weight gain in these two ethnic groups. However, the effects of life style including diet and exercise cannot be excluded. Copyright © 2007 John Wiley & Sons, Ltd. [source] DNA damage in metabolic syndrome and its association with antioxidative and oxidative measurementsINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 10 2006R. DEMIRBAG Summary The purpose of this study was to assess DNA damage levels in subjects with metabolic syndrome (MetS). Sixty-five subjects with MetS and 65 controls were enrolled in this study. Levels of DNA damage, total antioxidant capacity (TAC), total peroxide and oxidative stress index (OSI) were measured. We found that DNA damage levels were significantly increased [155.5 (60,264) vs. 93.2 (0,208) arbitrary units; p < 0.001] and TAC levels were significantly decreased in MetS than in control (1.34 ± 0.27 vs. 55 ± 0.33 mmol Trolox equivalent/l; p < 0.001). A significant falling trend in TAC levels and a significant rising trend in DNA damage values with the increase in the number of metabolic disturbances (anova p < 0.001 for both) were observed. Total peroxide (30.9 ± 4.9 vs. 21.3 ± 2.5 ,mol H2O2/l; p < 0.001) and OSI levels [2.4 (1.3,3.8) vs. 1.4 (0.7,2.3) arbitrary units; p < 0.001] were significantly higher in the subjects with MetS than in controls. We found significant negative correlation between DNA damage and TAC levels in MetS (r = ,0.656, p < 0.001) and in control (r = ,0.546, p < 0.001). In multiple linear regression analysis, age, body mass index, presence of MetS and number of the componens of MetS were independent predictors of log-transformed DNA damage (p < 0.05, for all). DNA damage is increased in patients with MetS. The increase in DNA damage might be occur because of the increase in the imbalance between the production of oxidants and antioxidant defences in subjects with MetS. [source] Stereological comparison of 3D spatial relationships involving villi and intervillous pores in human placentas from control and diabetic pregnanciesJOURNAL OF ANATOMY, Issue 2 2000TERRY M. MAYHEW In human placenta, 3D spatial relationships between villi and the maternal vascular bed determine intervillous porosity and this, in turn, influences haemodynamics and transport. Recently-developed stereological methods were applied in order to examine and quantify these relationships. Placentas were collected after 37 wk from control pregnancies and those associated with maternal diabetes mellitus classified according to duration and severity (White classification scheme). Two principal questions were addressed: (1) are normal spatial arrangements maintained in well-controlled diabetes mellitus? and (2) do arrangements vary between diabetic groups? To answer these questions, tissue sections cut at random positions and orientations were generated by systematic sampling procedures. Volume densities of villi (terminal+intermediate), intervillous spaces and perivillous fibrin-type fibrinoid deposits were estimated by test point counting and converted to global volumes after multiplying by placental volumes. Design-based estimates of the sizes (volume- and surface-weighted volumes) of intervillous ,pores' were obtained by measuring the lengths of point- and intersection-sampled intercepts. From these, theoretical numbers of pores were calculated. Model-based estimates (cylinder model) of the hydraulic diameters and lengths of pores were also made. Second-order stereology was used to examine spatial relationships within and between villi and pores and to test whether pair correlation functions deviated from the value expected for ,random' arrangements. Estimated quantities did not differ significantly between diabetic groups but did display some departures from control values in non-insulin-dependent (type 2) diabetic placentas. These findings support earlier studies which indicate that essentially normal microscopical morphology is preserved in placentas from diabetic subjects with good glycaemic control. Therefore, it is likely that fetal hypoxia associated with maternal diabetes mellitus is due to metabolic disturbances rather than abnormalities in the quantities or arrangements of maternal vascular spaces. [source] Metabolic syndrome, insulin resistance, and periodontitis: a cross-sectional study in a middle-aged French populationJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 7 2010Catherine Benguigui Benguigui C, Bongard V, Ruidavets J-B, Chamontin B, Sixou M, Ferrières J, Amar J. Metabolic syndrome, insulin resistance and periodontitis: a cross-sectional study in a middle-aged French population. J Clin Periodontol 2010; 37: 601,608. doi: 10.1111/j.1600-051X.2010.01571.x. Abstract Aim: Metabolic syndrome consists of a cluster of clinical and biological abnormalities, influenced by insulin resistance and promoting cardiovascular diseases. We examined the relationships between metabolic syndrome, its various components, insulin resistance, and periodontitis. Materials and Methods: The study included 276 subjects (35,74 years) recruited within a cross-sectional survey on cardiovascular risk factors. Twenty-one were excluded because of infectious risk or total tooth loss. Clinical attachment loss (CAL), probing pocket depth (PD), gingival and plaque indexes were recorded. Periodontitis was classified into moderate and severe forms. Results: The mean age was 58, 41% of the subjects had moderate and 39% had severe periodontitis. In univariate comparisons, periodontitis was associated with metabolic syndrome (p=0.050), most of its components, and HOMA index (homoeostasis model assessment of insulin resistance). After adjustment for confounders, only HOMA index remained associated with severe periodontitis (odds ratio [OR]=3.97 [95% confidence interval: 1.22,12.9], OR=3.78 [1.14,12.5] for third and fourth versus the first quartile of the HOMA index, respectively). The HOMA index was also associated with the number of periodontal sites with CAL4 mm, CAL5 mm, or PD4 mm (greater number for higher HOMA-index values). This relationship disappeared in never-smokers. Conclusions: Our data support the relationships between metabolic disturbances and periodontitis, with a central role of insulin resistance. [source] Intersection between metabolic dysfunction, high fat diet consumption, and brain agingJOURNAL OF NEUROCHEMISTRY, Issue 2 2010Romina M. Uranga J. Neurochem. (2010) 114, 344,361. Abstract Deleterious neurochemical, structural, and behavioral alterations are a seemingly unavoidable aspect of brain aging. However, the basis for these alterations, as well as the basis for the tremendous variability in regards to the degree to which these aspects are altered in aging individuals, remains to be elucidated. An increasing number of individuals regularly consume a diet high in fat, with high-fat diet consumption known to be sufficient to promote metabolic dysfunction, although the links between high-fat diet consumption and aging are only now beginning to be elucidated. In this review we discuss the potential role for age-related metabolic disturbances serving as an important basis for deleterious perturbations in the aging brain. These data not only have important implications for understanding the basis of brain aging, but also may be important to the development of therapeutic interventions which promote successful brain aging. [source] Acupuncture in Polycystic Ovary Syndrome: Current Experimental and Clinical EvidenceJOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2008E. Stener-Victorin This review describes the aetiology and pathogenesis of polycystic ovary syndrome (PCOS) and evaluates the use of acupuncture to prevent and reduce symptoms related with PCOS. PCOS is the most common female endocrine disorder and it is strongly associated with hyperandrogenism, ovulatory dysfunction and obesity. PCOS increases the risk for metabolic disturbances such as hyperinsulinaemia and insulin resistance, which can lead to type 2 diabetes, hypertension and an increased likelihood of developing cardiovascular risk factors and impaired mental health later in life. Despite extensive research, little is known about the aetiology of PCOS. The syndrome is associated with peripheral and central factors that influence sympathetic nerve activity. Thus, the sympathetic nervous system may be an important factor in the development and maintenance of PCOS. Many women with PCOS require prolonged treatment. Current pharmacological approaches are effective but have adverse effects. Therefore, nonpharmacological treatment strategies need to be evaluated. Clearly, acupuncture can affect PCOS via modulation of endogenous regulatory systems, including the sympathetic nervous system, the endocrine and the neuroendocrine system. Experimental observations in rat models of steroid-induced polycystic ovaries and clinical data from studies in women with PCOS suggest that acupuncture exert long-lasting beneficial effects on metabolic and endocrine systems and ovulation. [source] New approaches to parenteral nutrition in infants and childrenJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5 2002RG Heine Abstract: Parenteral nutrition (PN) has become a mainstay in the treatment of children with intestinal failure or conditions that preclude enteral feeding. Estimated energy and protein requirements can usually be met, unless the patient is fluid volume restricted or glucose intolerant. Although PN is generally well tolerated, in some patients it is still associated with a significant morbidity. Complications include metabolic disturbances, venous access device infection or dysfunction, venous thrombosis and cholestatic liver disease. Patients need to be carefully monitored for evidence of micronutrient deficiencies or excesses. There is a close relationship between line sepsis and thrombosis. Strict aseptic technique is the key to preventing line infections. Recurrent sepsis and thrombosis may eventually lead to loss of venous access and may jeopardize the long-term delivery of PN. Chronic cholestatic liver disease is common in premature infants with gastrointestinal problems, recurrent sepsis and lack of enteral feeding. The aetiology is multifactorial. Early enteral feeding is the most effective strategy in preventing PN-associated liver disease. New specialized nutrient solutions and lipid emulsions promise improved clinical outcomes. However, long-term clinical data are not yet available in children. In recent years, nutrition support teams have improved clinical and economic outcomes by encouraging the appropriate use and monitoring of PN therapy. In patients with intestinal failure, parent-administered home PN has become an alternative to long-term hospitalization. Apart from a positive effect on the quality of life of patient and family, home PN is cost-effective and reduces the risk of nosocomial infections and catheter-related complications. [source] Bilateral occipital neuropathy as a rare complication of positioning for thyroid surgery in a morbidly obese patientACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2004S. Schulz-Stübner Background:, Peripheral neuropathies in various locations are described as complications after anesthesia and surgery. This is the first case report of temporary bilateral occipital neuropathy from positioning for thyroid surgery in a morbidly obese patient. Methods:, A 48-year-old women with a history of depression, fibro-myalgia, asthma, sleep apnea, diabetes mellitus and morbid obesity (127 kg, 165 cm) underwent 4 hours anesthesia with propofol/remifentanil without muscle relaxation for thyroid surgery. The neck with a very low range of motion secondary to fat tissue needed to be extended to facilitate surgery as much as possible. The head was carefully padded and there were no episodes of hypotension or hypoxemia throughout the case or in the PACU. At post op day 1 she complained of bilateral numbness in the distribution area of both greater occipital nerves. On post op day 2 tingling sensations and improvement of numbness was noticed. The patient recovered without residual symptoms after 6 weeks. Conclusion:, Pressure or shear stress to the nerve, hypoperfusion or metabolic disturbances are discussed as the leading etiology of nerve damage during surgery in the literature. Pressure from fat tissue during prolonged head extension for surgery seems to be the cause in this case and should therefore be avoided whenever possible in morbidly obese patients, especially when other risk factors for neuropathy like diabetes are present. [source] Caffeine impairs intramuscular energy balance in patients susceptible to malignant hyperthermiaMUSCLE AND NERVE, Issue 3 2003Zoran Textor MD Abstract Malignant hyperthermia (MH) is a metabolic myopathy with an abnormal release of calcium by the sarcoplasmic reticulum (SR), triggered by volatile anesthetics and succinylcholine. Similarly, caffeine enhances Ca2+release by the SR in vitro. In a prospective, randomized study, high-energy phosphates were studied by intramuscular 31-phosphorus magnetic resonance spectroscopy (31P-MRS) in 10 MH-susceptible (MHS) and 7 MH-nonsusceptible (MHN) subjects before and after injection of 0.5 ml caffeine (20 mM). Intramuscular energy balance, measured by the ratios of Pi/PCr and Pi/,-ATP, did not differ between MHS and MHN patients before and after intramuscular caffeine injection. However, within each group, Pi/PCr and Pi/,-ATP increased significantly only in the MHS group. Intramuscular caffeine injection seemed to impair the metabolic balance in MHS individuals. This may reflect a local calcium overload leading to consumption of high-energy phosphates and increase of inorganic phosphate. Intramuscular stimulation by caffeine and 31P-MRS may provide a valuable tool to investigate MH-related metabolic disturbances. Muscle Nerve 28: 353,358, 2003 [source] Social stress, visceral obesity, and coronary artery atherosclerosis: product of a primate adaptationAMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009Carol A. Shively Abstract Abdominal obesity is prevalent and often accompanied by an array of metabolic perturbations including elevated blood pressure, dyslipidemia, impaired glucose tolerance or insulin resistance, a prothrombotic state, and a proinflammatory state, together referred to as the metabolic syndrome. The metabolic syndrome greatly increases coronary heart disease (CHD) risk. Social stress also increases CHD although the mechanisms through which this occurs are not completely understood. Chronic stress may result in sustained glucocorticoid production, which is thought to promote visceral obesity. Thus, one hypothesis is that social stress may cause visceral fat deposition and the metabolic syndrome, which, in turn increases CHD. CHD is caused by coronary artery atherosclerosis (CAA) and its sequelae. Cynomolgus monkeys (Macaca fascicularis) are a well-established models of CAA. Social subordination may be stressful to cynomolgus monkeys and result in hypercortisolemia and exacerbated CAA in females. Herein is reviewed a body of literature which suggests that social stress increases visceral fat deposition in cynomolgus monkeys, that subordinate females are more likely than dominants to have visceral obesity, that females with visceral obesity have behavioral and physiological characteristics consistent with a stressed state, and that females with high ratios of visceral to subcutaneous abdominal fat develop more CAA. While these relationships have been most extensively studied in cynomolgus macaques, obesity-related metabolic disturbances are also observed in other primate species. Taken together, these observations support the view that the current obesity epidemic is the result of a primate adaptation involving the coevolution with encephalization of elaborate physiological systems to protect against starvation and defend stored body fat in order to feed a large and metabolically demanding brain. Social stress may be engaging these same physiological systems, increasing the visceral deposition of fat and its sequelae, which increase CHD risk. Am. J. Primatol. 71:742,751, 2009. © 2009 Wiley-Liss, Inc. [source] ECG Manifestations of Multiple Electrolyte Imbalance: Peaked T Wave to P Wave ("Tee-Pee Sign")ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009Amer M. Johri M.D. The surface electrocardiogram (ECG) is a useful instrument in the detection of metabolic disturbances. The accurate characterization of these disturbances, however, may be considerably more difficult when more than one metabolic abnormality is present in the same individual. While "classic" ECG presentations of common electrolyte disturbances are well described, multiple electrolyte disturbances occurring simultaneously may generate ECG abnormalities that are not as readily recognizable. We report a case of hyperkalemia, with concurrent hypocalcemia and hypomagnesemia resulting in (1) peaking of the T wave, (2) a prominent U wave, and (3) prolongation of the descending limb of the T wave such that it overlapped with the next P wave. In this particular ECG from a patient with combined electrolyte imbalance, we have dubbed the unusual appearance of the segment between the peak of the T wave to the next P wave as the "tee-pee" sign. [source] Determination of the time required for appropriate chemical de-epithelialization of an ileal segment for cystoplasty: an animal modelBJU INTERNATIONAL, Issue 6 2005Jalal Bakhtiari Another group of authors from Iran attempted experimentally to determine the required time for the appropriate enzymatic treatment of the ideal segment to complete de-epithelialization, thus reducing its absorptive function. They found that 25 min of enzymatic treatment of the ideal segment was adequate for this, and that it was recommended from their experimental study for cystoplasty. OBJECTIVES To determine the time required for the appropriate enzymatic treatment of an ileal segment to de-epithelialize its mucosa and to reduce its absorptive function for cystoplasty in dogs. MATERIALS AND METHODS Twenty-one adult female Persian mixed-breed dogs were divided into seven equal groups: group 1 (negative control group) had no ileocystoplasty; group 2 (positive control group) had a routine ileocystoplasty with no enzymatic treatment of the ileal segment; and groups 3,7 had an ileocystoplasty with 5, 10, 15, 20 or 25 min, respectively, of enzymatic treatment of the ileal segment with collagenase and trypsin. The seven groups were then compared for haematological, biochemical and histological changes, and glucose reabsorption assessed using a glucose-absorption test. RESULTS No dogs showed any signs of metabolic disturbances, biochemical and haematological changes. There were significant differences in blood glucose level (BGL) for the groups at different times after the glucose-absorption test, but a pair-wise comparison showed significant differences in BGL between group 1 and the other groups, except group 7. The degree of histopathological change was associated with the duration of enzymatic treatment, in that changes were more prominent in group 7. There was no shrinkage or collagen deposition. CONCLUSIONS In these conditions, 25 min of enzymatic treatment of the ileal segment is sufficient to remove the absorptive function of the augmented bladder, and is recommended for cystoplasty in dogs. [source] Combination treatment with telmisartan and hydrochlorothiazide in black patients with mild to moderate hypertensionCLINICAL CARDIOLOGY, Issue 1 2001Janet B. Mcgill M.D. Abstract Background: Hydrochlorothiazide (HCTZ) is commonly used to treat black patients with hypertension. To avoid the metabolic disturbances associated with high-dose HCTZ, blood pressure control may be achieved by combining low doses with another antihypertensive. Hypothesis: The study was undertaken to assess the tolerability and antihypertensive dose-response efficacy of telmisartan and HCTZ and their combination in black patients with mild to moderate hypertension (mean supine blood pressure 140/95-200/114 mmHg). Methods: Following a 4,week, single-blind, placebo run-in period, 222 black patients were randomized to once-daily treatment with one of 20 different double-blind combinations of telmisartan (0, 20, 40, 80, 160 mg) and HCTZ (0, 6.25, 12.5, 25 mg) for 8 weeks. Blood pressure was measured at baseline and after 2, 4, and 8 weeks. Results: Telmisartan 80 mg/HCTZ 12.5 mg reduced supine trough diastolic blood pressure (DBP),primary efficacy parameter,by 13.3 mmHg, and supine trough systolic blood pressure (SBP) by 21.5 mmHg. These reductions represented benefits of 13.7/8.7 mmHg over telmisartan 80 mg and 12.3/8.1 mmHg over HCTZ 12.5 mg(p<0.01). Telmisartan 40 mg/HCTZ 12.5 mg reduced supine trough SBP/DBP by 14.3/10.0 mmHg, amounting to 12.3/3.3 mmHg more than telmisartan 40 mg and 5.1/4.8 mmHg more than HCTZ 12.5 mg, This reached significance for the comparisons with telmisartan 40 mg for SBP and HCTZ 12.5 mg for DBP (p,0.05). A response surface analysis and therapeutic response rates confirmed the additive antihypertensive effects of telmisartan and HCTZ. All treatments were well tolerated, with side-effect profiles comparable with placebo. Adverse events were mainly transient and of mild to moderate severity. Conclusions: Telmisartan 80 mg combined with HCTZ 12.5 mg is effective and well tolerated in black patients with mild to moderate hypertension, providing greater antihypertensive activity than the corresponding monotherapies. [source] Is veno-venous bypass still needed during liver transplantation?CLINICAL TRANSPLANTATION, Issue 1 2009A review of the literature Abstract:, Orthotopic liver transplantation has been made feasible with intra-operative femoral-to-jugular veno-venous bypass (VVB) to redirect the blood from the lower extremities and the kidneys to the heart. This reduces hemodynamic instability and metabolic disturbances. However, complications such as thromboses with pulmonary thrombembolism or post-reperfusion syndrome were observed in up to 30% of the cases. The latter, recent developments of cava-sparing surgical techniques, shorter anhepatic times plus optimized anesthetic management have made the necessity for a routine use of VVB questionable. [source] | ||||||||||||||||||||||||||||